I'm a little confused by your question. Additionally, I'm not sure that glaucoma is associated with tunnel vision. Glaucoma is an increase in intra ocular pressure and leads to damage of retinal ganglion cells. Is this selective to peripheral ganglion cells? Not sure this is the case. Secondly, not sure what you mean by neural remapping. The brain already does a fair amount of filling in of blind spots, naturally. For example, RP patients usually don't know they have a problem until significant degeneration as already occurred. The visual cortex already does a phenomenal job at correcting for retinal degenerative problems.

Thanks Alan,

I have modified the explanation as per your concern. I was under the impression (perhaps mistakenly) that damage to the retina characteristic of people with tunnel vision was sometimes consequent upon high intra ocular pressure.

Please please have a look at the attached file and you will see exactly what I mean.

Nope, you're right. Tunnel vision can occur in glaucoma. Wonder why this is? Perhaps because of a thinner layer of ganglion cells in the periphery?

Cheers Alan!

Tunnel vision indeed occurs in glaucoma and in some types of retinitis pigmentosa (RP). In addition to what mentioned by Sam, there is also a "redundancy theory" to explain the tunnel vision. It is assumed in the theory that there is a diffuse loss of retinal ganglion cells (RGCs) in glaucoma. Since there is more functional redundancy (meaning the same function is carried out by more than one RGCs) in the central visual fields than peripheral ones, you will have more functional deficit in peripheral fields and the central ones once diffuse loss of RGCs occurs.

Is anyone at all interested in the attachment??????????

Tunnel vision occurs in Retinitis Pigmentosa (RP) and also in the final stages of glaucoma. Rod photoreceptors which are present in peripheral retina whereas cones are present in the fovea which is for about 10 degrees of central visual fields. Since RP affects preferentially the Rods therefore their destruction results in tunnel vision.

But the explanation of tunnel vision in later stages of glaucoma is very confusing based on the present theories of raised IOP, cupping and neurodegenerative disease in the causation of glaucoma. Textbooks state that the RGCs or their axons are being destroyed in glaucoma due to raised IOP or due to pre-programmed apoptosis but they don’t talk about the real crucial issue in glaucoma: What ever the cause of glaucoma may be: the bottom line is that the nerve fibers are always being destroyed in an orderly fashion starting with the peripheral fibers and ending with the central fibers and never destroy haphazardly. I fail to understand: why don’t we take into account the orderly destruction of nerve fibers in glaucoma? I would like to discuss the present theories of glaucoma in the context of orderly destruction of nerve fibers, and my colleagues may decide for themselves whether my arguments make any sense or not.

Can raised IOP acting directly can destroy the nerve fibers in an orderly fashion in glaucoma

Unlikely. How is it possible that raised IOP acting directly will always destroy the peripheral fibers first and never destroy them randomly? Answer to this question may tell us that the any role of raised IOP acting directly on the nerve fibers is invalid

Can the concept of cupping explain the orderly destruction of nerve fibers in glaucoma?

Unlikely. The term cupping implies that the physiological cups start enlarging due to raised IOP in glaucoma. Term cupping was originally given by Heinrich Muller in 1856 which unfortunately has become synonymous with glaucoma. The concept of cupping has been unable to answer many puzzling questions.

According to Wolf’s anatomy, the different size physiological cups are produced by the varying degree of atrophy of the Bergmeister papilla (BP), a tuft of hyaloid vessels supplying nutrition to the lens in fetal life. If the physiological cups are fibrous tissue remnant of BP then why should they get enlarge concentrically in glaucoma? Why shouldn’t the cups get deeper due to raised IOP instead of enlarging concentrically? Moreover, why is the lamina not being pushed outward instead of bowing posteriorly due to raised IOP. I don’t have answers to these questions.

My most puzzling question about cupping. the nerve fibers originating closest to the disc lie most superficial (closest to vitreous) and exit from the most central part of the disc. Therefore, these central fibers should be destroyed first resulting in concentric enlargement of the blind spot and not the initial loss of peripheral fibers if cupping was indeed occurring in glaucoma. Cupping may explain orderly destruction of nerve fibers in glaucoma but their destruction would be other way around. The central fibers should be destroyed first and the peripheral fibers at the end if cupping was indeed but occurring in glaucoma, but the nerve fibers are being destroyed in the reverse order. I believe the term cupping was mistakenly given 150 years ago.

Can the nerve fibers be destroyed in an orderly fashion if glaucoma is a neurodegenerative disease?

Unlikely. If glaucoma is a neurodegenerative disease, then our genes must first have predicted the impending glaucoma so to initiate apoptosis invariably and precisely with those RGC’s which serve the peripheral vision and ending with central vision in an orderly fashion, an unlikely scenario.


I don’t believe our genes are smart enough to have such an extraordinary predictive capability. If the nerve fibers are being destroyed in an orderly fashion in glaucoma, then we should expect the mechanism for their destruction to be an orderly too—which can’t occur in a neurodegenerative disease.

Then, why are the nerve fibers being destroyed in an orderly fashion in glaucoma?

I hypothesize that optic disc may be sinking and as a result the nerve fibers are being stretched and broken. Due to sinking of the disc the peripheral fibers would be the first to be stretched and broken, whatever we may call it. As the disc sinking advances the next in line nerve fibers would move towards the periphery to occupy the vacant space and thus also get severed against the scleral edge. This process would continue until the central nerve fibers are also severed and the disc area becomes totally empty. End-stage glaucomatous disc may not be 100% cupped disc but a left over disc area after all the nerve fibers have been severed. Moreover, It is not only the nerve fibers but the blood vessels are also been severed which would explain the occurrence of hemorrhages at the disc margin. Sinking of the disc and severing of the nerve fibers should and is able to answer all the unanswered questions in glaucoma. Bottom line: the nerve fibers are being severed, not atrophied in glaucoma. Glaucoma may not be an optic disc neuropathy but an optic disc axotomy- paradigm shift. Thanks for your time.